Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2007-12-10
pubmed:abstractText
In an attempt to define mechanisms by which B-cell non-Hodgkin lymphoma (NHL) may escape rituximab immunotherapy, we developed several rituximab-resistant cell lines (RRCL) generated from the rituximab-sensitive cell lines (RSCL) Raji and RL. Rituximab resistance was associated with CD20 downregulation and upregulation of CD52 and the complement inhibitory proteins (CIPs) CD55 and CD59. No significant alemtuzumab-associated complement-mediated cell lysis (CMC) or antibody-dependent cellular cytotoxicity (ADCC) was demonstrated in RSCL. In contrast, in vitro exposure of RRCL to alemtuzumab resulted in a significant degree of CMC and ADCC. Of note, in vitro blocking of CD52 with anti-CD52 F(ab')(2) fractions in RRCL improved rituximab-associated CMC as compared to unblocked RRCL. Our current data provides a basis for further evaluation of alemtuzumab-based clinical trials for patients with rituximab-resistant NHL.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal, http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal, Humanized, http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal..., http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Neoplasm, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD20, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Neoplasm, http://linkedlifedata.com/resource/pubmed/chemical/Antineoplastic Agents, http://linkedlifedata.com/resource/pubmed/chemical/CD52 antigen, http://linkedlifedata.com/resource/pubmed/chemical/Complement System Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Glycoproteins, http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class II, http://linkedlifedata.com/resource/pubmed/chemical/alemtuzumab, http://linkedlifedata.com/resource/pubmed/chemical/rituximab
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1042-8194
pubmed:author
pubmed:issnType
Print
pubmed:volume
48
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2424-36
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:18067019-Antibodies, Monoclonal, pubmed-meshheading:18067019-Antibodies, Monoclonal, Humanized, pubmed-meshheading:18067019-Antibodies, Monoclonal, Murine-Derived, pubmed-meshheading:18067019-Antibodies, Neoplasm, pubmed-meshheading:18067019-Antibody-Dependent Cell Cytotoxicity, pubmed-meshheading:18067019-Antigens, CD, pubmed-meshheading:18067019-Antigens, CD20, pubmed-meshheading:18067019-Antigens, Neoplasm, pubmed-meshheading:18067019-Antineoplastic Agents, pubmed-meshheading:18067019-Apoptosis, pubmed-meshheading:18067019-Cell Line, Tumor, pubmed-meshheading:18067019-Complement System Proteins, pubmed-meshheading:18067019-Cytotoxicity, Immunologic, pubmed-meshheading:18067019-Drug Resistance, Neoplasm, pubmed-meshheading:18067019-Glycoproteins, pubmed-meshheading:18067019-Histocompatibility Antigens Class II, pubmed-meshheading:18067019-Humans, pubmed-meshheading:18067019-Lymphoma, Non-Hodgkin
pubmed:year
2007
pubmed:articleTitle
CD52 over-expression affects rituximab-associated complement-mediated cytotoxicity but not antibody-dependent cellular cytotoxicity: preclinical evidence that targeting CD52 with alemtuzumab may reverse acquired resistance to rituximab in non-Hodgkin lymphoma.
pubmed:affiliation
Department of Medicine, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural